Defects in iron absorption and utilization lead to iron deficiency and overload disorders. Adult mammals absorb iron through the duodenum, whereas embryos obtain iron through placental transport. Iron uptake from the intestinal lumen through the apical surface of polarized duodenal enterocytes is mediated by the divalent metal transporter, DMT1 (Fleming, M. D., et al., Nature Genet., 16:383–386, 1997; Gunshin, H., et al., Nature, 388:482–488, 1997; Andrews, N.C., N. Engl. J. Med., 341:1986–1995, 1999). A second transporter has been postulated to export iron across the basolateral surface to the circulation. The function of this iron transporting protein may be perturbed in mammalian disorders of iron deficiency or overload. Drugs to alter the function of this iron transporting protein may be useful to treat such diseases as hemochromatosis and some forms of anemia.